Search

Background: Arthrofibrosis is a debilitating postoperative complication of total knee arthroplasty (TKA). It is one of the leading causes of hospital readmission and a predominant reason for TKA failure. The prevalence of arthrofibrosis will increase as the annual incidence of TKA in the United States rises into the millions.Methods: In a narrative review of the literature, the etiology, economic burden, treatment strategies, and future research directions of arthrofibrosis after TKA are examined.Results: Characterized by excessive proliferation of scar tissue during an impaired wound healing response, arthrofibrotic stiffness causes functional deficits in activities of daily living. Postoperative, supervised physiotherapy remains the first line of defense against the development of arthrofibrosis. Also, adjuncts to traditional physiotherapy such as splinting and augmented soft tissue mobilization can be beneficial. The effectiveness of rehabilitation on functional outcomes depends on the appropriate timing, intensity, and progression of the program, accounting for the patient's ability and level of pain. Invasive treatments such as manipulation under anesthesia, debridement, and revision arthroplasty improve range of motion, but can be traumatic and costly. Future studies investigating novel treatments, early diagnosis, and potential preoperative screening for risk of arthrofibrosis will help target those patients who will need additional attention and tailored rehabilitation to improve TKA outcomes.Conclusion: Arthrofibrosis is a multi-faceted complication of TKA, and is difficult to treat without an early, tailored, comprehensive rehabilitation program. Understanding the risk factors for its development and the benefits and shortcomings of various interventions are essential to best restore mobility and function. [ABSTRACT FROM AUTHOR]

Background: Diabetic forefoot joint deformities are a known risk factor for skin breakdown and amputation, but the causes of deformity are not well understood. The purposes of this study were to determine the effects of intrinsic foot muscle deterioration and limited ankle joint mobility on the severity of metatarsophalangeal joint (MTPJ) deformity, and determine the relationships between these potential contributing factors and indicators of diabetic complications (peripheral neuropathy and advanced glycation end products). Methods: A total of 34 participants with diabetic neuropathy (average age, 59 years; range 41-73) were studied. MTPJ angle and intrinsic foot muscle deterioration were measured with computed tomography and magnetic resonance imaging, respectively. Maximum ankle dorsiflexion was measured using kinematics. Skin intrinsic fluorescence served as a proxy measure for advanced glycation end product accumulation. Results: Total forefoot lean muscle volume (r = −0.52, P < .01) and maximum ankle dorsiflexion (r = −0.42, P < .05) were correlated with severity of MTPJ deformity. Together they explained 35% of the variance of MTPJ angle. Neuropathy was correlated with forefoot muscle deterioration (ρ = 0.53, P < .01). Skin intrinsic fluorescence was correlated to severity of neuropathy (r = 0.50, P < .01) but not maximum ankle dorsiflexion, or forefoot deterioration when controlling for neuropathy. Conclusion: These results suggest that the interplay of intrinsic foot muscle deterioration and limited ankle mobility may be the primary contributor to the development of MTPJ deformity. Identifying these muscle and ankle motion impairments as risk factors for MTPJ deformity supports the need for targeted interventions early in the disease process to slow, or possibly stop the progression of deformity over time and reduce the risk of amputation. Level of Evidence: Level IV, case series. [ABSTRACT FROM AUTHOR]